A case of Brunner's gland hyperplasia: endoscopic color Doppler ultrasonographic findings.
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Brunner Glands↗
Biomedical subjects
K Kihira
Publications and source records attributed to K Kihira.
The value of LYM-1 cells for examining vacuole formation and loss of cell viability induced by culture supernates of Helicobacter pylori.
Some strains of Helicobacter pylori are known to produce an extracellular cytotoxin that causes vacuolation in cultured mammalian cells. Screening for such strains makes use of HeLa cells which may not be sensitive enough to detect minimal changes. The aim of this study was to develop a more sensitive cell line. Vacuole formation was examined in HeLa cells, as well as four other cell lines established in this laboratory by ammonium chloride induction. Among five cell lines tested, LYM-1 cells were most sensitive for the detection of intracellular vacuolation with this agent. Loss of cell viability of LYM-1 and HeLa cells induced by H. pylori culture supernates was also examined: LYM-1 were more sensitive than HeLa cells. Cell death was not always accompanied by vacuole formation. This suggests that the mechanism whereby cell death occurs must be different from that for vacuole formation. LYM-1 cells may be useful when measuring vacuole formation and cell death of the cultured cells induced by culture supernates of clinical isolates of H. pylori.
Ammonium Chloride↗
The efficacy and safety of one-week triple therapy with lansoprazole, clarithromycin, and metronidazole for the treatment of Helicobacter pylori infection in Japanese patients.
BACKGROUND: The aim of this study was to evaluate the efficacy and tolerability of 1-week, low-dose triple therapy with lansoprazole, clarithromycin, and metronidazole (LCM) for the cure of H. pylori infection and to establish the adequate dosage of a new triple therapy for Japanese patients. MATERIALS AND METHODS: One hundred four H. pylori-positive Japanese patients were assigned alternatively to one of two groups: one to receive either 30 mg lansoprazole once in the morning, 200 mg clarithromycin twice daily, and 250 mg metronidazole twice daily for 1 week (LCM1; n = 52); the other to receive 30 mg lansoprazole once in the morning, 200 mg clarithromycin twice daily, and 500 mg metronidazole twice daily for 1 week (LCM2; n = 52). H. pylori infection was assessed by smear, culture, and histological assessment (Giemsa stain) performed before and 4 weeks after cessation of the therapy. RESULTS: The overall cure rates of H. pylori infection were 92.3% (48 of 52; 95% confidence interval (CI), 85% to 100%) in LCM1 and 92.3% (48 of 52; 95% CI, 85% to 100%) in LCM2. The cure rates in the patients without prior treatment were 95.7% (44 of 46; 95% CI, 89%-100%) in LCM1 and 95.7% (45 of 47; 95% CI, 89%-100%) in LCM2. Minor side effects were observed in 7.7% of LCM1 and 9.6% of LCM2, respectively. CONCLUSION: The LCM1 regimen consisting of 30 mg lansoprazole once daily, 200 mg clarithromycin twice daily, and 250 mg metronidazole twice daily (the regular doses in ordinary use in Japan) is a highly effective and safe regimen for Japanese patients. LCM1 as a new triple therapy is a promising regimen for the first-line treatment of H. pylori infection in Japanese patients.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Deficiencies of automatic endoscopic reprocessors: a method to achieve high-grade disinfection of endoscopes.
BACKGROUND: We show that disinfection using the automatic endoscopic reprocessor is not complete and propose a method for high-grade disinfection of endoscopes. METHODS: We used an automatic endoscopic reprocessor, Pyser System 83, and 2% glutaraldehyde. After each endoscopic procedure, the endoscopes were divided into three groups. Endoscopes in group A were washed only by the reprocessor. Group B endoscopes were washed by the reprocessor after the connectors were soaked in glutaraldehyde for 5 minutes. The channels, valves, connecting sections of group C endoscopes, and the connectors of the machine were sprayed with glutaraldehyde before machine-washing. Swabs were taken from all 13 parts of each endoscope and machine for microbiologic culture. RESULTS: Six endoscopes were positive, cumulatively, for bacterial contamination in group A. Among group B endoscopes, one remained contaminated. No endoscope was positive in group C. The difference between group A and C was statistically significant (p < .05). CONCLUSIONS: Machine washing by automatic endoscopic reprocessors may not achieve complete disinfection. Additional procedures are necessary. High-grade disinfection of the connectors is critical. Disinfection of the interface between the connectors is important.
Disinfection↗
Distribution of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis.
OBJECTIVES: To investigate the extent of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis. METHODS: Endoscopy with biopsies from the lesser curvatures of the antrum, angulus, middle body, and the greater curvature of the middle body of the stomach was performed in 59 patients with histologically confirmed chronic gastritis. The extent of atrophic gastritis was assessed endoscopically as well histologically. H. pylori status was assessed by histology as well as enzyme-linked immunosorbent assay. The histological severity of chronic and acute inflammation, glandular atrophy, and intestinal metaplasia was assessed according to the Sydney system. RESULTS: In H. pylori-positive patients, H. pylori was evenly distributed throughout the stomach when the extent of atrophic gastritis was limited to the antrum and the lesser curvature of the body, but disappeared from the antrum of patients with more extensive atrophic gastritis. The severity of acute and chronic inflammation at the greater curvature of the body increased with the extension of atrophic gastritis. In H. pylori-negative patients, the severity of chronic inflammation at the greater curvature of the body was significantly higher in patients with extensive atrophic gastritis than in those with a lesser extent of atrophic gastritis. CONCLUSION: At the greater curvature of the body, the development of atrophy is closely associated with the increase in the severity of inflammation, which is more marked in H. pylori-positive patients.
Adolescent↗
Effect of some sulfonate analogues of ursodeoxycholic acid on biliary lipid secretion in the rat.
The effect of the sulfonate analogues of ursodeoxycholic acid, namely sodium 3 alpha,7 beta-dihydroxy-24-nor-5 beta-cholane-23-sulfonate (norUDC-SO3Na) and sodium 3 alpha, 7 beta-dihydroxy-5 beta-cholane-24-sulfonate (UDC-SO3Na), on biliary lipid secretion was studied in bile fistula rats. During intravenous infusion of the two sulfonate analogues, bile flow and biliary lipid secretion were stimulated in a dose-dependent manner. This suggests that the analogues exert an effect on biliary lipid secretion comparable to that of the naturally occurring bile acid, ursodeoxycholyltaurine (UDC-tau). The effects of norUDC-SO3Na and UDC-SO3Na on bile flow were similar but slightly smaller than that of UDC-tau. The output of bile salts was similar with both sulfonates but greater than that with UDC-tau. The infusion of norUDC-SO3Na or UDC-SO3Na induced cholesterol secretion and phospholipid secretion more significantly than UDC-tau infusion. The increase in phospholipid secretion was particularly pronounced during high-dose administration of norUDC-SO3Na. Although norUDC-SO3Na stimulated cholesterol secretion more intensely than the other two bile salts, it also facilitated phospholipid output, perhaps as a compensatory mechanism, and the biliary cholesterol/phospholipid ratio was decreased to a greater extent by the sulfonates than by UDC-tau. Consequently, the administration of norUDC-SO3Na or UDC-SO3Na produces a more "stable" bile than UDC-tau, suggesting that these sulfonates possess potential cholelitholytic activity.
Animals↗
15 alpha-hydroxylation of a bile acid analogue, sodium 3 alpha,7 alpha-dihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate in the hamster.
The metabolism of 3 alpha,7 alpha-dihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate (bishomoCDC-sul), the sulfonate analogue of bishomochenodeoxycholic acid, and its effect on biliary bile acid composition were studied during chronic administration in the hamster. After oral administration of radiolabeled bishomoCDC-sul, more than 80% of the radioactivity was excreted into the feces within 7 days, both as the unchanged sulfonate (38.5%) and two more polar metabolites (50.0% and 11.5%). The half time of the fecal excretion was 1.6 days. In gallbladder bile, the unchanged sulfonate and its major metabolite accounted for 19.1% and 19.8% of total bile acids, respectively. In another experiment, hamsters were fed bishomoCDC-sul with antibiotics to evaluate the site of biotransformation. Even when the number of intestinal microorganisms was greatly reduced, the same three metabolites were found in the feces: bishomoCDC-sul (44.0%) and the two polar metabolites (30.8% and 25.1%). The major metabolite was isolated from feces of the hamsters fed bishomoCDC-sul without antibiotics. Its chemical structure was identified by mass spectrometry and nuclear magnetic resonance spectroscopy as the 15 alpha-hydroxylated derivative, namely sodium 3 alpha,7 alpha,15 alpha-trihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate. These results indicate that after oral administration, the sulfonate analogue of bishomochenodeoxycholic acid underwent enterohepatic circulation like a natural bile acid and was transformed, in part, into the 15 alpha-hydroxylated derivative and another more polar metabolite in the liver of hamsters. There was no evidence that bishomoCDC-sul was dehydroxylated to a lithocholic acid analogue during enterohepatic cycling.
Animals↗
Early recognition of patients with decreased methotrexate clearance following high-dose methotrexate infusion therapy.
The purpose of this study was to identify the patients with decreased methotrexate (MTX) clearance as early as possible after the start of high-dose methotrexate (HD-MTX) infusion. Fifty-six patients (age: 18 approximately 83 years) received a HD-MTX infusion (dosage: 1.9 approximately 3.8 g/m2) for 6 h. These patients were retrospectively divided into a low-clearance group and a high-clearance group based on the serum MTX concentration at 48 h (1 microM). Six out of the 56 patients showed decreased MTX clearance. The MTX concentrations in the low-clearance group were significantly higher than those in the high-clearance group even in earlier sampling times than at 48 h. The average MTX concentrations were 330 microM at 6 h, 72 microM at 12 h, and 16 microM at 24 h in the low-clearance group, and those in the high-clearance group were 210 microM, 18 microM, and 1.0 microM, respectively. The estimated elimination half-lives (t1/2) at 6 approximately 12 h and 12 approximately 24 h after the start of the infusion were also significantly longer in the low-clearance group (2.8 vs. 1.7 h and 5.0 vs. 2.8 h, respectively). Therefore, we proposed convenient criteria based on the mean + 1 S.D. of the high-clearance group: the concentration > 270 microM at 6 h and > 32 microM at 12 h; the t1/2 value > 2.1 h at 6-12 h. All 6 patients were recognized as belonging to the low-clearance group at an early stage after HD-MTX infusion by using our proposed criteria. These results indicate that patients with decreased MTX clearance could be identified within the first 12 h after the start of HD-MTX infusion. The factors influencing the prolonged elimination of MTX were also investigated. A significant decrease in renal function on day 2 was observed in the low-clearance group. The MTX level at 12 h and the estimated t1/2 values were significantly correlated with BUN, Scr and Clcr on the 2nd day after HD-MTX therapy, suggesting that an alteration in renal function occurs within 12 h of the HD-MTX infusion. The prolonged elimination of MTX could be attributable to this decrease in renal function.
Adult↗
Simple 13C-urea breath test with infra-red spectrophotometer.
When mass spectrophotometric analysis is used for the 13C-urea breath test to assess H. pylori infection, it is costly, complicated, and time-consuming. To overcome these disadvantages, we utilized an infra-red spectrophotometer as a substitute for the mass spectrophotometer. A total of 153 patients (181 tests) analyzed with peptic ulcers or non-ulcer dyspepsia were investigated. Breath samples were collected 15 min after ingestion of 13C-urea (100 mg in 30 ml water). An infra-red spectrophotometer was used to determine the concentration of 13CO2 in the expirate. The 13CO2/12CO2 ratio was also measured by mass spectrophotometry to compare results with those of infra-red spectrophotometric analysis. Direct detection of H. pylori was qualified in biopsy specimens. Of the 181 biopsies, 138 were positive for H. pylori infection and 43 were negative. With the urea breath test, the mean value in the positive group was significantly higher than that in the negative group (0.062 +/- 0.044 vs 0.011 +/- 0.014, respectively). The cut-off level, 0.01, was determined as delta 13C atom %. The sensitivity of infra-red spectrophotometry was 97.8% (135/138) and specificity was 74.4% (32/43). There was an extremely high coefficient of correlation (r = 0.996) between mass and infra-red photometric analysis. Infra-red spectrometry appears to have great potential not only for diagnosing H. pylori infection but also for assessing treatment results. Its advantages include technical simplicity, cost-effectiveness, and high accuracy.
Breath Tests↗
Efficacy of clarithromycin in eradicating Helicobacter pylori.
We reviewed reports on the efficacy of clarithromycin in eradicating Helicobacter pylori. Reports on dual and 1-week triple therapy that included clarithromycin were analyzed to assess the eradication rates of H. pylori infection. Dual therapy with clarithromycin and a proton pump inhibitor achieved eradication rates of 38%-83%, and 1-week triple therapy with omeprazole, clarithromycin, and other antibiotics achieved eradication rates, of 80%-96%. The incidence of side effects with all regimens was low. Clarithromycin is useful for treatment of H. pylori infection. One-week triple therapy that includes clarithromycin and a proton pump inhibitor effectively eradicates H. pylori.
Anti-Bacterial Agents↗
Endoscopic topical therapy for the treatment of Helicobacter pylori infection.
We modified a novel topical therapeutic method for the treatment of Helicobacter pylori infection to increase its effectiveness and tolerability. Sixty-six patients (with nonulcer dyspepsia, inactive ulcer, or active ulcer) were given lansoprazole (30 mg, h.s.) and pronase (18,000 tyrosine units, b.i.d.) orally for 2 days before the topical therapy. One hundred milliliters of 7% sodium bicarbonate solution containing bismuth subnitrate, amoxicillin, metronidazole (at two different regimens), and pronase was instilled into the stomach through an endoscope. A double-lumen tube with a balloon at the tip was inserted into the duodenum along with the endoscope. The balloon was inflated with 25 ml of air and was lodged postbulbarly. The solution was kept in the stomach for 2 h, and the patient's position was changed every 15 min from the sitting to the supine, prone, and right lateral position, each position being maintained twice, to expose the entire gastric mucosa. The solution was aspirated at the end of the procedure. H. pylori infection was cured in 16/22 (72.7%) of patients with nonulcer dyspepsia, in 21/26 (80.7%) of patients with inactive ulcer, and in 1/18 (5.6%) patients with active ulcer. H. pylori eradication was confirmed 4 weeks after the therapeutic procedure by smear, culture, and histology of antral and corpus biopsy specimens. Side effects (loose stools) were observed in two patients only, and one patient had loss of appetite. These effects were transient. This endoscopic topical therapy for H. pylori infection is a safe, effective, and well tolerated procedure. With further modifications of the drug regimens and the method itself, this procedure could be of interest as anti-H. pylori therapy.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Synthesis and metabolism of sodium 3 alpha,7 alpha-dihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate in the hamster.
This paper reports the chemical synthesis of a new bile acid analogue, namely sodium 3 alpha,7 alpha-dihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate (bishomoCDC-sul) from chenodeoxycholic acid and describes its metabolism in the hamster. The structure of the new compound was confirmed by proton and carbon-13 nuclear magnetic resonance spectroscopy. After intravenous infusion of [3H]-labeled sulfonate into bile fistula hamsters, it was extracted by the liver and secreted into the bile; more than 65% of the radioactivity was recovered in the bile within 1 h. Following intraduodenal administration of the [3H]sulfonate and [14C]chenodeoxycholyltaurine, both compounds were excreted into the bile more slowly; only 41 and 43% of the radioactivity, respectively, were recovered in the bile during the four-hour experimental period. In contrast, when the labeled compounds were injected into the terminal ileum, both the sulfonate and chenodeoxycholyltaurine were rapidly absorbed and secreted into the bile; 84 and 97%, respectively, of the radioactivity were recovered during a four-hour period. Chromatographic analysis demonstrated that in these short-term experiments most (> 95%) of the sulfonate was secreted into the bile without biotransformation regardless of the route of administration. When infused intravenously at increasing doses, bishomoCDC-sul induced cholestasis at an infusion rate of 1 mumol/min/kg. These results suggest that sodium 3 alpha,7 alpha-dihydroxy-25,26-bishomo-5 beta-cholane-26-sulfonate was absorbed from the terminal ileum by active transport, extracted by the liver, and secreted into the bile in a manner similar to that of the natural bile acids.
Animals↗
Determination of the glucurono-conjugated position in bile alcohol glucuronides present in a patient with cerebrotendinous xanthomatosis.
The determination of the glucurono-conjugated position in three bile alcohol glucuronides secreted in bile of a patient with cerebrotendinous xanthomatosis was carried out by a nuclear magnetic resonance study. The bile sample was extracted with ethanol and chromatographed on an ion-exchange column, a reverse-phase partition column and a silica gel column to isolate glucurono-conjugates of 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol, 5 beta-cholestane-3 alpha, 7 alpha 12 alpha, 23-tetrol, and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 23, 25-pentol. Proton and 13C nuclear magnetic resonance spectra of the two biliary bile alcohol glucuronides, 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol glucuronide and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 23, 25-pentol glucuronide were identical with those of the synthetic glucuronide 7 alpha, 12 alpha, 25-trihydroxy-5 beta-cholestane-3 alpha-O beta-D-glucopyranosyluronic acid and the isolated glucuronide 3 alpha, 7 alpha, 12 alpha, 25-tetrahydroxy-5 beta-cholestane-23-O-beta-D-glucopyranosyluronic acid from urine of a patient with cerebrotendinous xanthomatosis, respectively. Hence, the glucurono-conjugated positions of the biliary 25-tetrol glucuronide and the biliary 23,25-pentol glucuronide were C-3 and C-23, respectively. By comparison of the 13C chemical shift data with that of the unconjugated bile alcohol, 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 23-tetrol, the glucurono-conjugated position of the natural 23-tetrol glucuronide was determined to be C-23. Thus, the natural 23-tetrol glucuronide can be formulated as 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestane-23-O-beta-D-glucopyranosyluronic acid.
Bile↗
Efficacy of lansoprazole in eradication of Helicobacter pylori.
Fifty-eight Helicobacter pylori-positive ulcer patients received omeprazole 20 mg (n = 15), or lansoprazole 30 mg (n = 23), lansoprazole 60 mg (n = 13), or E3810 20 mg (n = 7) q.d. Another 63 H. pylori-positive ulcer patients received lansoprazole and clarithromycin for 2 weeks. Patients received lansoprazole 30 mg and clarithromycin 400 mg (group 1, n = 22), lansoprazole 30 mg and clarithromycin 800 mg (group 2, n = 12), or lansoprazole 60 mg and clarithromycin 800 mg (group 3, n = 29). Neither proton pump inhibitor (PPI) was capable of eradication by monotherapy, but the clearance rates in the lansoprazole group were 60.9 and 69.2%, which were higher than those for omeprazole (p < 0.05). In the dual therapy, eradication rates were 50, 50, and 72.4% in groups 1, 2, and 3, respectively. Minor side effects were observed in one case each in groups 1 and 3. Lansoprazole monotherapy proved more efficacious than omeprazole monotherapy, but it was unable to eradicate H. pylori. Dual therapy with lansoprazole 60 mg and clarithromycin 800 mg was an efficacious and safe regimen for H. pylori eradication in this study.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Effects of L-dopa on cholecystokinin octapeptide tissue levels in normal and 6-hydroxydopamine-treated rat brain.
We investigated the changes in cholecystokinin octapeptide (CCK8) tissue levels after the intraperitoneal administration of L-3,4-dihydroxyphenylalanine (L-dopa) in normal and 6-hydroxydopamine (6-OHDA) treated rat brains to clarify the interaction between CCK8 and dopamine (DA). The administration of L-DOPA to the normal rats elevated the regional CCK8-like immunoreactivity (CCK8LI) tissue levels in a dose dependent manner in the frontal cortex, striatum, and nucleus accumbens where CCK neurons were closely associated with DA neurons but not in the hippocampus where CCK neurons were identified as local circuit neurons. Moreover, coadministration of D2-selective antagonist, L-sulpiride, with L-dopa inhibited the elevation of CCK8LI levels in several brain regions. This evidence indicates that CCK8 release was inhibited by exogenous DA converted from L-dopa via D2 receptor stimulation. In the 6-OHDA treated rats on the 3rd day after the treatment, the L-dopa administration elevated the CCK8 levels in several regions. However, the elevation of CCK8LI levels was not observed on the 7th day after the 6-OHDA treatment. These results suggest that there would be a great difference in the effect of L-DOPA on CCK8LI levels between the 3rd day and 7th day after 6-OHDA treatment. It was concluded that the changes in CCK8LI levels would be due to changes in CCK8 release, and that the CCK8 release would be regulated by extracellular DA via D2 receptor.
Animals↗
Regional characteristics of [125I]cholecystokinin octapeptide specific binding to rat brain membranes following 6-hydroxydopamine treatment.
The relative changes in the amount of specific [125I]cholecystokinin octapeptide (CCK8) bound to regional brain membrane preparations after 6-hydroxydopamine (6-OHDA) treatment were examined. The specific binding in the frontal cortex and striatum decreased and reached a minimum on the 3rd day after 6-OHDA treatment. Thereafter, the specific binding recovered to 60% and 65% of control values in the frontal cortex and striatum respectively on the 28th day. On the other hand, in the nucleus accumbens, where CCK8 co-exists in the dopamine neuron, the specific binding decreased gradually, and its recovery was delayed compared with that of the frontal cortex and striatum. In the hippocampus, 6-OHDA treatment had no effect on the specific binding throughout the experimental period. The decrease of [125I]CCK8-specific binding could be caused by enhanced release of CCK8 in the frontal cortex, striatum, and nucleus accumbens, and the recovery of specific binding could be induced by depletion of CCK8 in nerve terminals. Particularly in the nucleus accumbens, the delayed recovery of specific binding suggests the loss of the pre-synaptic binding site, which exists in the CCK8/DA co-existing neuron, together with a change in CCK8 release.
Animals↗
[A case report of colon cancer in ulcerative colitis followed up for 9 years after the detection of high-grade dysplasia on biopsy].
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Biopsy↗
A 1-h topical therapy for the treatment of Helicobacter pylori infection.
OBJECTIVE: A novel topical therapeutic methodology for the treatment of Helicobacter pylori infection was developed and studied in 25 patients with H. pylori to evaluate safety and efficacy. METHODS: The patients had been given lansoprazole (30 mg, hs) orally and pronase (18,000 tyrosine units, b.i.d.) for the 2 days before topical therapy. One hundred milliliters of solution with 80 ml of 7% sodium bicarbonate and 20 ml of contrast medium meglumine sodium amidotrizoate containing bismuth subnitrate (1 g), amoxicillin (2 g), metronidazole (1 g), and pronase (36,000 tyrosine units) were instilled into the stomach through a nasally introduced 16-Fr intestinal tube with a balloon at its radiopaque tip, which was inflated with approximately 25 ml of air and lodged postbulbarly at the superior duodenal angle under fluoroscopy, thus preventing leakage of the solution distally into the jejunum. The solution was kept in the stomach for 1 h, and the patient's position was changed every 15 min from the sitting to the supine, prone, and right lateral position to expose the entire gastric mucosa. The solution was suctioned at the end of the procedure. RESULTS: H. pylori infection was successfully cured in 24 (96%) patients, confirmed 4 wk after the therapeutic procedure by negative smear, culture, and histology of the antral and corpus biopsy specimens. No side effects were observed except for loose stools in one case. CONCLUSION: This 1-h topical therapy is a safe, effective, and well tolerated procedure for the treatment of H. pylori infection. With further improvements and modifications of the method itself, as well as of the drug regimens, this method may become a highly efficient modality for anti-H. pylori therapy.
Adult↗